scholarly journals Variable Dopamine Release Probability and Short-Term Plasticity between Functional Domains of the Primate Striatum

2003 ◽  
Vol 23 (10) ◽  
pp. 4378-4385 ◽  
Author(s):  
Stephanie J. Cragg
Keyword(s):  
Dopamine Release ◽  
Functional Domains ◽  
Short Term ◽  
Short Term Plasticity ◽  
Release Probability

scholarly journals Presynaptic Endoplasmic Reticulum Contributes Crucially to Short-term Plasticity in Small Hippocampal Synapses

2018 ◽  
Author(s):  
Nishant Singh ◽  
Thomas Bartol ◽  
Herbert Levine ◽  
Terrence Sejnowski ◽  
Suhita Nadkarni
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Influx ◽  
Critical Role ◽  
Presynaptic Terminal ◽  
Calcium Stores ◽  
Pathological State ◽  
Calcium Dynamics ◽  
Short Term ◽  
Short Term Plasticity ◽  
Release Probability

Short-term plasticity (STP) of the presynaptic terminal maintains a brief history of activity experienced by the synapse that may otherwise remain unseen by the postsynaptic neuron. These synaptic changes are primarily regulated by calcium dynamics in the presynaptic terminal. A rapid increase in intracellular calcium is initiated by the opening of voltage-dependent calcium channels in response to depolarization, the main source of calcium required for vesicle fusion. Separately, electron-microscopic studies of hippocampal CA3-CA1 synapses reveal the strong presence of endoplasmic reticulum (ER) in all presynaptic terminals. However, the precise role of the ER in modifying STP at the presynaptic terminal remains unexplored. To investigate the contribution of ER in modulating calcium dynamics in small hippocampal boutons, we performed in silico experiments in a physiologically-realistic canonical synaptic geometry based on reconstructions of CA3-CA1 Schaffer collaterals in the rat hippocampus. The model predicts that presynaptic calcium stores are critical in generating the observed paired-pulse ratio (PPR) of normal CA3-CA1 synapses. In control synapses with intact ER, SERCA pumps act as additional calcium buffers, lowering the intrinsic release probability of vesicle release and increasing PPR. In addition, the presence of ER allows ongoing activity to trigger calcium influx from the presynaptic ER via ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs). Intracellular stores and their associated machinery also allows a synapse with a low release probability to operate more reliably due to attenuation of calcium fluctuations. Finally, blocking ER activity in the presynaptic terminal mimics the pathological state of a low facilitating synapse characterized in animal models of Alzheimer’s disease, and underscores the critical role played by presynaptic stores in normal function.

scholarly journals Rapid regulation of vesicle priming explains synaptic facilitation despite heterogeneous vesicle:Ca2+ channel distances

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Janus RL Kobbersmed ◽  
Andreas T Grasskamp ◽  
Meida Jusyte ◽  
Mathias A Böhme ◽  
Susanne Ditlevsen ◽  
...  
Keyword(s):  
Super Resolution ◽  
Release Site ◽  
Stochastic Simulations ◽  
Short Term ◽  
Short Term Plasticity ◽  
Release Probability ◽  
Vesicular Release ◽  
Dependent Inhibition ◽  
Super Resolution Microscopy ◽  
Activity Dependent

Chemical synaptic transmission relies on the Ca2+-induced fusion of transmitter-laden vesicles whose coupling distance to Ca2+ channels determines synaptic release probability and short-term plasticity, the facilitation or depression of repetitive responses. Here, using electron- and super-resolution microscopy at the Drosophila neuromuscular junction we quantitatively map vesicle:Ca2+ channel coupling distances. These are very heterogeneous, resulting in a broad spectrum of vesicular release probabilities within synapses. Stochastic simulations of transmitter release from vesicles placed according to this distribution revealed strong constraints on short-term plasticity; particularly facilitation was difficult to achieve. We show that postulated facilitation mechanisms operating via activity-dependent changes of vesicular release probability (e.g. by a facilitation fusion sensor) generate too little facilitation and too much variance. In contrast, Ca2+-dependent mechanisms rapidly increasing the number of releasable vesicles reliably reproduce short-term plasticity and variance of synaptic responses. We propose activity-dependent inhibition of vesicle un-priming or release site activation as novel facilitation mechanisms.

scholarly journals Plasticity in striatal dopamine release is governed by release-independent depression and the dopamine transporter

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Mark D. Condon ◽  
Nicola J. Platt ◽  
Yan-Feng Zhang ◽  
Bradley M. Roberts ◽  
Michael A. Clements ◽  
...  
Keyword(s):  
Dopamine Transporter ◽  
Dopaminergic Neurons ◽  
Action Potentials ◽  
Dopamine Release ◽  
Ex Vivo ◽  
Dorsal Striatum ◽  
Short Term ◽  
Fast Scan Cyclic Voltammetry ◽  
Short Term Plasticity ◽  
Initial Release

Abstract Mesostriatal dopaminergic neurons possess extensively branched axonal arbours. Whether action potentials are converted to dopamine output in the striatum will be influenced dynamically and critically by axonal properties and mechanisms that are poorly understood. Here, we address the roles for mechanisms governing release probability and axonal activity in determining short‐term plasticity of dopamine release, using fast‐scan cyclic voltammetry in the ex vivo mouse striatum. We show that brief short‐term facilitation and longer short term depression are only weakly dependent on the level of initial release, i.e. are release insensitive. Rather, short-term plasticity is strongly determined by mechanisms which govern axonal activation, including K+‐gated excitability and the dopamine transporter, particularly in the dorsal striatum. We identify the dopamine transporter as a master regulator of dopamine short‐term plasticity, governing the balance between release‐dependent and independent mechanisms that also show region‐specific gating.

scholarly journals Plasticity in striatal dopamine release is governed by release-independent depression and the dopamine transporter

2018 ◽  
Author(s):  
Mark D. Condon ◽  
Nicola J. Platt ◽  
Yan-Feng Zhang ◽  
Bradley M. Roberts ◽  
Michael A. Clements ◽  
...  
Keyword(s):  
Dopamine Transporter ◽  
Dopamine Release ◽  
Ex Vivo ◽  
Dorsal Striatum ◽  
List Type ◽  
Short Term ◽  
Fast Scan Cyclic Voltammetry ◽  
Short Term Plasticity ◽  
Initial Release ◽  
Axonal Excitability

AbstractMesostriatal DA neurons possess extensively branched axonal arbours. Whether action potentials are converted to DA output in striatum will be influenced dynamically and critically by axonal properties and mechanisms that are poorly understood. We addressed the roles for mechanisms governing release probability and axonal activity in determining short-term plasticity of DA release, using fast-scan cyclic voltammetry in ex vivo mouse striatum. Brief short-term facilitation (STF) and longer short-term depression (STD) were only weakly dependent on the level of initial release, i.e. were release-insensitive. Rather, short-term plasticity was strongly determined by mechanisms which governed axonal activation, including K+-gated excitability and the dopamine transporter (DAT), particularly in dorsal striatum. We identify the DAT as a master regulator of DA short-term plasticity, governing the balance between release-dependent and independent mechanisms that also show region-specific gating.Key FindingsShort-term plasticity in dopamine release is only weakly governed by initial releaseShort-term depression is strongly dependent on axonal excitability and activationThe dopamine transporter controls short-term plasticity and drives short-term depressionDopamine transporters govern the balance between release-dependent and -independent mechanisms

scholarly journals Regulation of a subset of release-ready vesicles by the presynaptic protein Mover

2021 ◽  
Vol 118 (3) ◽  
pp. e2022551118
Author(s):  
Ermis Pofantis ◽  
Erwin Neher ◽  
Thomas Dresbach
Keyword(s):  
Synaptic Vesicles ◽  
Wild Type ◽  
Short Term ◽  
Calyx Of Held ◽  
Short Term Plasticity ◽  
Release Probability ◽  
Pulse Ratio ◽  
Vesicular Release ◽  
Evolutionarily Conserved ◽  
Presynaptic Protein

Neurotransmitter release occurs by regulated exocytosis from synaptic vesicles (SVs). Evolutionarily conserved proteins mediate the essential aspects of this process, including the membrane fusion step and priming steps that make SVs release-competent. Unlike the proteins constituting the core fusion machinery, the SV protein Mover does not occur in all species and all synapses. Its restricted expression suggests that Mover may modulate basic aspects of transmitter release and short-term plasticity. To test this hypothesis, we analyzed synaptic transmission electrophysiologically at the mouse calyx of Held synapse in slices obtained from wild-type mice and mice lacking Mover. Spontaneous transmission was unaffected, indicating that the basic release machinery works in the absence of Mover. Evoked release and vesicular release probability were slightly reduced, and the paired pulse ratio was increased in Mover knockout mice. To explore whether Mover’s role is restricted to certain subpools of SVs, we analyzed our data in terms of two models of priming. A model assuming two SV pools in parallel showed a reduced release probability of so-called “superprimed vesicles” while “normally primed” ones were unaffected. For the second model, which holds that vesicles transit sequentially from a loosely docked state to a tightly docked state before exocytosis, we found that knocking out Mover selectively decreased the release probability of tight state vesicles. These results indicate that Mover regulates a subclass of primed SVs in the mouse calyx of Held.

scholarly journals Release probability modulates short‐term plasticity at a rat giant terminal

2000 ◽  
Vol 524 (2) ◽  
pp. 513-523 ◽  
Author(s):  
Sharon Oleskevich ◽  
John Clements ◽  
Bruce Walmsley
Keyword(s):  
Short Term ◽  
Short Term Plasticity ◽  
Release Probability

scholarly journals Regulation of synaptic release-site Ca2+ channel coupling as a mechanism to control release probability and short-term plasticity

FEBS Letters ◽  
2018 ◽  
Vol 592 (21) ◽  
pp. 3516-3531 ◽  
Author(s):  
Mathias A. Böhme ◽  
Andreas T. Grasskamp ◽  
Alexander M. Walter
Keyword(s):  
Control Release ◽  
Release Site ◽  
Short Term ◽  
Channel Coupling ◽  
Short Term Plasticity ◽  
Release Probability ◽  
Synaptic Release

Short term plasticity of the primary sensory cortex revealed by interventions contralateral to the stimulus in Median nerve SEP

2006 ◽  
Vol 37 (01) ◽  
Author(s):  
T Waberski ◽  
A Dieckhöfer ◽  
U Reminghorst ◽  
H Buchner ◽  
R Gobbelé
Keyword(s):  
Median Nerve ◽  
Sensory Cortex ◽  
Short Term ◽  
Short Term Plasticity ◽  
Primary Sensory Cortex
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